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This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 104/2/321    most recent 00442.2007v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Boissiere, J. Articles by Bonnet, P. Search for Related Content PubMed PubMed Citation Articles by Boissiere, J. Articles by Bonnet, P.

Moderate exercise training does not worsen left ventricle remodeling and function in untreated severe hypertensive rats

¹Laboratoire de Physiopathologie de la Paroi Artérielle, Université François Rabelais, UFR Médecine, Tours; and ²Laboratoire Interuniversitaire de Biologie de l'Activité Physique et Sportive, Université Clermont-Ferrand, France

Submitted 24 April 2007 ; accepted in final form 20 November 2007

Exercise training and hypertension induced cardiac hypertrophy but modulate differently left ventricle (LV) function. This study set out to evaluate cardiac adaptations induced by moderate exercise training in normotensive and untreated severe hypertensive rats. Four groups of animals were studied: normotensive (Ctl) and severe hypertensive (HT) Wistar rats were assigned to be sedentary (Sed) or perform a moderate exercise training (Ex) over a 10-wk period. Severe hypertension was induced in rat by a two-kidney, one-clip model. At the end of the training period, hemodynamic parameters and LV morphology and function were assessed using catheterism and conventional pulsed Doppler echocardiography. LV histology was performed to study fibrosis infiltrations. Severe hypertension increased systolic blood pressure to 202 ± 9 mmHg and induced pathological hypertrophy (LV hypertrophy index was 0.34 ± 0.02 vs. 0.44 ± 0.02 in Ctl-Sed and HT-Sed groups, respectively) with LV relaxation alteration (early-to-atrial wave ratio = 2.02 ± 0.11 vs. 1.63 ± 0.12). Blood pressure was not altered by exercise training, but arterial stiffness was reduced in trained hypertensive rats (pulse pressure was 75 ± 7 vs. 62 ± 3 mmHg in HT-Sed and HT-Ex groups, respectively). Exercise training induced eccentric hypertrophy in both Ex groups by increasing LV cavity without alteration of LV systolic function. However, LV hypertrophy index was significantly decreased in normotensive rats only (0.34 ± 0.02 vs. 0.30 ± 0.02 in Ctl-Sed and Ctl-Ex groups, respectively). Moreover, exercise training improved LV passive filling in Ctl-Ex rats but not in Ht-Ex rats. In this study, exercise training did not reduce blood pressure and induced an additional physiological hypertrophy in untreated HT rats, which was slightly blunted when compared with Ctl rats. However, cardiac function was not worsened by exercise training.

renal hypertension; cardiac function